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USP19 activates Endoplasmic Reticulum Stress. 5 / 5
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"Our study reveals that USP19 elevates the intracellular Ca 2+ concentration to alter ER stress via regulation of BAG6 and BCL2 stability and may be a viable therapeutic target for TNBC therapy."
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"Histological and immunohistochemical (IHC) analyses found that USP19 enhanced the expression of ER stress‐related proteins to induce the ER stress response (Figure 7E)."
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"Taken together, these results indicated that USP19 can induce the activation of ER stress‐related apoptosis through stabilization of BAG6 expression levels, thereby ameliorating TNBC progression in vivo.3.8 METTL14 reduced m 6 A RNA methylation of USP19 ."
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"Knockdown of BAG6 in mice also reversed ER stress triggered by USP19, indicating that the essential effects of USP19 on ER stress depend on BAG6 stability."
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"Collectively, USP19 can significantly increase the unfolded protein entering the ER and induce ER stress, by reducing BAG6 ubiquitination to kill TNBC cells.m A methylation had received a lot of attention recently and was now widely acknowledged as the most frequent and prolific alteration on mRNA and as a mechanism to control RNA translation, stability, and degradation."
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